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1 Biomedical Sciences, New York College of Osteopathic Medicine / NYIT, Old Westbury, New York, United States
2 Anatomy and Cell Biology, University of Iowa, Iowa City, Iowa, United States
3 Cardiology, Univ. Iowa, United States
4 Institut de Recherches Internationales Servier, Courbevoie, France
* To whom correspondence should be addressed. E-mail: ededkov{at}nyit.edu.
We tested the hypothesis that chronically reducing the heart rate in infarcted middle-aged rats using ivabradine (IVA) would induce arteriolar growth and attenuate perivascular collagen and, thereby, improve maximal perfusion and coronary reserve in the surviving myocardium. Myocardial infarction (MI) was induced in 12-month-old male Sprague-Dawley rats, which were then treated either with IVA (10.5 mg/kg/day; MI+IVA) or placebo (MI) via i.p. osmotic pumps for 4 weeks. Four weeks of IVA treatment limited the increase in left ventricular end-diastolic pressure and the decrease in ejection fraction, but did not affect the size of the infarct, the magnitude of myocyte hypertrophy, or the degree of arteriolar and capillary growth. However, treatment reduced interstitial and periarteriolar collagen in the surviving myocardium of MI+IVA rats. The reduced periarteriolar collagen content was associated with improvement in maximal myocardial perfusion and coronary reserve. Although the rates of proliferation of periarteriolar fibroblasts were similar in the MI and MI+IVA groups, the expression levels of the AT1 and TGF
1 in the myocardium, as well as the level of the Ang II peptide in the plasma, were lower in treated rats 14 days after MI. Therefore, our data reveal that improved maximal myocardial perfusion and coronary reserve in MI+IVA rats most likely the result of reduced periarteriolar collagen rather than enhanced arteriolar growth.
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